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目的 初步探讨地佐环平 (MK 80 1)对脑缺血的保护作用与兴奋性氨基酸 (EAA)和抑制性氨基酸(IAA)释放的关系。方法 营养液中去除糖和氧 ,建立大鼠脑突触体缺血模型 ,检测静息及高钾去极化状态下 ,缺血突触体EAA和IAA释放量及游离钙浓度。结果 大鼠突触体缺血状态致天冬氨酸和甘氨酸、牛磺酸、γ 氨基丁酸释放量明显增加 ,而谷氨酸亦有增加趋势。缺血 + 5 0mmol·L- 1K+刺激后 ,上述EAA及IAA释放量均进一步增加。静息及去极化状态下的缺血突触体游离钙浓度显著增加。MK 80 10 .1mmol·L- 1可显著阻遏静息及去极化状态缺血突触体释放EAA及IAA ,但对EAA的抑制作用更明显 ;同时亦明显降低两种状态下缺血突触体内游离钙浓度。结论 MK 80 1的抗脑缺血致脑损伤作用 ,至少部分与其对抗缺血引起的突触体内游离钙浓度升高和EAA释放量增加的作用有关。
Objective To investigate the protective effect of MK 80 1 on cerebral ischemia and its relationship with the release of excitatory amino acids (EAA) and inhibitory amino acids (IAA). Methods Saccharomyces cerevisiae and oxygen were removed from the nutrient solution. Rat cerebral synaptosomal ischemia model was established. The release of EAA and IAA and the free calcium concentration of ischemic synaptosome under resting and high potassium depolarization conditions were measured. Results The release of aspartate and glycine, taurine and γ-aminobutyric acid from the synaptosomal ischemic state of rats increased significantly, while glutamate also increased. Isotonic + 5 0 mmol·L-1 K + stimulation, the EAA and IAA release were further increased. There was a significant increase in ischemic synaptosome free calcium concentration at rest and depolarization. MK 80 10 .1 mmol·L -1 significantly inhibited the release of EAA and IAA from resting and depolarized ischemic synaptosomes, but inhibited the EAA more obviously. Meanwhile, it also significantly reduced the ischemic synapse In vivo free calcium concentration. Conclusions The anti-ischemic brain damage induced by MK 80 1 is at least partly related to the anti-ischemic effect of increased intracellular free calcium concentration and EAA release.